AI Article Synopsis
- The SCY1-like (SCYL) family, specifically SCYL1, has been linked to cancer metastasis, but its role in gastric cancer (GC) remains unclear until this study.
- Researchers analyzed SCYL1 expression in GC using various databases and clinical samples, finding that higher SCYL1 levels correlated with worse patient outcomes.
- SCYL1 was found to enhance GC cell migration and invasion while inhibiting autophagy, indicating it activates the mTORC1 signaling pathway, suggesting it could be a target for future treatments of gastric cancer.
Article Abstract
Background: The SCY1-like (SCYL) family has been reported to be closely related to cancer metastasis, but it has not been reported in gastric cancer (GC), and its specific mechanism is not clear.
Methods: We utilized databases like Deepmap, TCGA, and GEO to identify SCYL1's role in GC. Clinical samples were analyzed for SCYL1 expression and its correlation with patient prognosis. In vitro and in vivo experiments were conducted to assess SCYL1's function in GC cell migration, invasion, and autophagy.
Results: SCYL1 showed an increased expression in GC tissues, which correlated with a negative prognosis. In vitro experiments demonstrated that SCYL1 promotes GC cell migration and invasion and inhibits autophagy. GSEA indicated an inverse relationship between SCYL1 and autophagy, while a direct relationship was observed with the mTORC1 signaling pathway. Knockdown of SCYL1 enhanced autophagy, while activation of mTORC1 reversed this effect.
Conclusions: SCYL1 is a significant contributor to GC progression, promoting metastasis by activating the mTORC1 signaling pathway and inhibiting autophagy. These findings suggest SCYL1 as a potential therapeutic target for GC treatment.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469978 | PMC |
| http://dx.doi.org/10.1007/s00432-024-05938-5 | DOI Listing |
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